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Thyroid Gland Dysfunctions: Assessment, Analysis, and Associated Dental Management Guidelines

THE THYROID GLAND

Thyroid Hormones

Thyroid follicles secreting hormones include:

• Thyroxine/Tetraiodothyronine (T4): T4 accounts for 90% of thyroid gland secretions and is the “inactive” version of thyroid hormone.
• Triiodothyronine (T3): T3 is the “active” version of thyroid hormone. Low T3 levels trigger TSH (Thyroid Stimulating Hormone) release from the pituitary, causing active conversion of T4 to T3. TSH levels drop when adequate T3 levels are achieved.
• Calcitonin: The C cells of the follicles produce calcitonin (CT) in response to higher-than-normal concentrations of calcium ions in the extracellular fluids. Calcitonin stimulates osteoblasts, inhibits osteoclasts, and slows the intestinal absorption and renal conservation of calcium ions.

Role of Thyroid Hormones

• Thyroid hormones stimulate energy production and utilization by peripheral cells.
• The follicle cells manufacture thyroglobulin and store it as a colloid, filling the lumen of the follicle. The cells also actively transport iodine from the extracellular fluids into the follicular chamber, where they complex with the thyroglobulin molecules. Reabsorbed thyroglobulin is broken down into amino acids and thyroid hormones; the hormones diffuse into the circulation.
• Most of the thyroid hormones entering the bloodstream are attached to special thyroid-binding globulins. Unbound hormones affect peripheral tissues at once; the binding globulins gradually release their hormones over a week or more.
• The primary regulatory mechanism involves the production of TSH by the anterior pituitary.
• Thyroid hormone also increases the sensitivity of the cardiovascular system to sympathetic nervous system activity, and this effect helps maintain a normal heart rate.

HYPERTHYROIDISM

Etiology

Graves’ disease is an autoimmune disorder associated with hyperthyroidism. The patient can present with hyperthyroidism due to a toxic nodular goiter, toxic adenoma, or exogenously, from excess thyroid hormone intake. Rarely, subacute thyroiditis (SAT) can cause temporary hyperthyroidism, which is associated with pain and tenderness over the thyroid area and with difficulty in swallowing.

Clinical Features

Hyperthyroidism can be associated with rapid heart rate, agitation, restlessness, anxiety, heat intolerance, fine tremors, polyphagia (excess appetite) with weight loss, excess perspiration involving the hands and feet, warm skin, menstrual irregularities, and frequent runs or diarrhea.

Graves’ disease is associated with proptosis or protruding eyes/exophthalmus because of infiltration of adipocytes and involvement of the Mueller’s muscles. This inflammation process can lead to double vision. The thyroid gland is firm and smooth in Graves’ disease. Graves’ disease patients can also have dermopathy that presents as pretibial myxedema or hypopigmentation of the skin.

Vital Signs and Cardiac Findings

The following are vital signs and cardiac findings for patients with hyperthyroidism:

• Pulse: The patient can have a rapid heart rate/tachycardia with irregular heartbeats and resting tachycardia, which is an increased pulse rate during sleep (the heart rate typically goes down during sleep in normal patients).
• Blood pressure: The systolic blood pressure (SBP) is elevated because the BMR is increased. The diastolic blood pressure (DBP) is decreased in the uncontrolled hyperthyroid patient. Thus, the pulse pressure (PP), which is the difference between the SBP and the DBP, is widened in uncontrolled hyperthyroidism and the PP is >40 mmHg (normal: 40 mmHg).
• Cardiac findings: Auscultation of the heart may often reveal a functional systolic murmur, which is a consequence of hyperdynamic circulation, secondary to the increased BMR and associated anemia. Arrhythmias can occur, and this is the reason why hyperthyroid patients often take digoxin (Lanoxin) and/or warfarin (Cou/>
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